Hepatic fibrosis, the accumulation of abnormal extracellular matrix (ECM) proteins and a resultant loss of liver function, is an accompaniment of an inflammation-driven wound healing process triggered by chronic liver injury. The main causes of liver injury leading to fibrosis in Western societies include chronic hepatitis C virus (HCV) infection, alcohol abuse, chronic hepatitis B (HBV) infection, iron overload as occurs in hereditary hemochromatosis, and increasingly, non-alcoholic steatohepatitis (NASH). The inflammatory process ensuing from hepatic injury triggers a variety of cellular responses including cell repair, hepatocyte regeneration, increased extracellular matrix turnover, and ultimately in some patients significant fibrosis. Progressive fibrosis of the liver eventually can result in cirrhosis, portal hypertension, liver failure, and hepatocelluar carcinoma.
Given the foregoing, it would be desirable to have methods of treating, preventing, and ameliorating fibrosis, such as fibrosis of the liver.